By

Dr. Jitendra Wadhwani

PG ORTHOPAEDICS
PGIMS, ROHTAK
 Zenker, a pathologist,1 st identified fat embolism
syndrome at autopsy 1862.

First diagnosed in 1873 by Dr Von Bergmann

1879 Fenger and Salisbury published description of

FES
Fat Emboli: Fat particles or droplets
that travel through the circulation

Fat Embolism: A process by which fat

emboli passes into the bloodstream
and lodges within a blood vessel.

Fat Embolism Syndrome (FES):

serious manifestation of fat
embolism occasionally causes multi
system dysfunction, the lungs are
always involved and next is brain
FAT EMBOLISM SYNDROME:

Clinical diagnosis, No specific laboratory test is

diagnostic

Mostly associated with long bone and pelvic #, and

more frequent in closed # then open #

Single long bone fracture 1-5% chance of

developing FES, and increases with number of #

Onset is 24-72 hours from initial insult

Mortality: 5-15%
CAUSES CONTD..
Blunt Trauma (90%)
CAUSES CONTD..
Non Trauma: agglutination of chylomicrons and VLDL
by high levels of plasma CRP.

disease-related
Diabetes, acute pancreatitis, burns, SLE, sickle cellcrisis

drug-related
parenteral lipid infusion

procedure-related
Orthopedic surgery, liposuction
Exact mechanism unknown, but two main hypothesis

Mechanical vs. Biochemical

MECHANICAL Fat globules from disrupted bone

marrow or adipose tissue are forced into torn venules
in areas of trauma.

BIOCHEMICAL Hormonal changes caused by trauma

and/or sepsis induce systemic release of free fatty
acids (FFA) as chylomicrons which cause the systemic
FES.
 Diagnosis is made CLINICALLY NOT
CHEMICALLY. It does not matter how much
fat globules are in your circulation, it just matters if
you have their side effects.

FES typically manifests 24 to 72 hours after the

initial insult. Rarely <12 hrs or >72 hrs.
TRIAD OF FES

Hypoxemia

Neurological abnormalities

Petechial rash
EARLY SIGNS

Dyspnea

Tachypnea

hypoxemia
PULMONARY:
Hypoxia, rales, pleural friction rub

Breath sounds: Loud harsh, Crepts & wheeze

ARDS may develop(fat emboli obstructs lung vessel

(20microns) platelets and fibrin adhere.)

of pts with FES require mechanical ventilation (Bulger,

Archives of Surgery 1997; 132: 435-9)

CXR usually normal early on, later may show

snowstorm pattern- diffuse bilateral infiltrates

CT chest: ground glass opacification with interlobular

septal thickening
NEUROLOGICAL FINDINGS:

Usually occur after respiratory symptoms.

Incidence 80% patients with FES
Minor global dysfunction most common, but ranges from
mild delirium to coma.
Seizures/focal deficits not common but can occur
Transient and reversible in most cases
CT Head: general edema, usually nonspecific
MRI brain: Low density on T1, and high intensity T2
signal, correlates to degree of impairment
RASH:
Petechial

Usually on conjuntiva , neck, axillae

Results from occlusion of dermal capillaries by fat

globules and then extravasations of RBC

Fleeting & last short.Resolves in 5-7 days

PATHOGNOMONIC, but only present in 20-50% of

patients
OTHER FINDINGS
Retinopathy (exudates, cotton wool spots, hemorrhage)
Lipiduria

Fever (to 39-40C)

DIC

Myocardial depression (prominent S, T depression, RBBB,

arrythmia)
Thrombocytopenia/Anemia
Hypocalcemia
DIAGNOSIS
FES is CLINICAL diagnosis, not biochemical.
A high degree of suspicion is needed to make diagnosis
.
-Common misconception that the presence of fat
globules, either in sputum, urine, or a wedged PA
catheter, is necessary to confirm the diagnosis of FES
In 50% of fracture patients, fat globules was
demonstrated in the serum, without symptoms of FES.
HOWEVER
Growing literature on the use of bronchoscopywith
bronchoalveolar lavage to detect fat droplets in alveolar
macrophages as a means to diagnose fat embolism.
Sensitivity and specificity are unknown, being studied in
Trauma patients
 FES = 1 major + 4 minor + fat microglobulinemia
Still widely used today
 FES = femur fracture tibia fracture + 1 feature
Based on respiratory parameters
3 TYPES- In 1962

SUBCLINICAL FES

NON FULMINANT FES

FULMINANT FES
SUBCLINICAL FES:

Around 3 days post trauma

Probably occurs in almost all long bone

fractures of the lower extremity and fractures of

the pelvis

Characterised by decreased PaO2, decreased

Hb% and decreased platelets. No clinical signs
and symptoms of respiratory insufficiency.
NONFULMINANT FES:

- Any time ,upto 6 days post trauma

-Clinical signs and symptoms are clearly evident.

Petechiae, tachycardia, respiratory failure, and signs of CNS

embolism.

Thrombocytopaenia, anaemia, and coagulation

abnormalities can be found, as can pulmonary alveolar and
interstitial opacities on chest x ray
 There is no definitive test for this version of the
syndrome, as most of the changes described can
occur as a result of trauma as well as a result of fat

embolism, the diagnosis remains a clinical one,

and the significance is uncertain
FULMINANT FES:
Occurs very suddenly and rapidly after injury, and
progresses very quickly, often resulting in death within a
few hours of the initial trauma.

Clinical features are acute respiratory failure, acute

cor pulmonale and embolic neurological changes.

These occur shortly after injury and often result in the

death of the patient.
 Pats. with multiple fractures are particularly
susceptible to this form of the syndrome, which,
although it is relatively rare, is of immense clinical
significance because of its high mortality.
TREATMENT IS LARGELY SUPPORTIVE

Constant Positive Airway pressure(CPAP)

Mechanical Ventilation

Antibiotics

Nutritional support

Corticosteroids

Heparins

Have all been used

INITIAL TREATMENT

Adequate airway

Start IV line correct fluid deficit

Basic investigation including baseline chest X-ray

and ABG assay (v. imp).
Nasogastric tube should be inserted in patient
with severe trauma and gastric contents suctioned
to prevent aspiration and ARDS
MONITORING

TPR, BP

I/O chart maintain output 50-100cc/hr

CVP to correct fluid deficit

If overload pulmn. Edema (4-8cm H2O)

Pulmonary haemodynamics PCWP for accurate mean

of deficit correction (5-12mm of Hg)

Arterial blood gas monitoring

SPECIFIC DRUG THERAPY:

Many drugs have tried, most without demonstrable

benefit in established ARDS except Corticosteroids
but with some prophylactic benefit.
Drugs which may be tried in Fat embolism associated
ARDS are:

1.Ethanol : Lipase inhibitor, low incidence when level

>20mg.
2.Heparin : PL aggregation useful in DIC assoc
ARDS also.Controversial in trials.10000-15000 iu stat &
10000 iu 4-6hly with PTT at 1.5-2.5 INR.

3.Hypertonic glucose: block post traumatic

mobilization of FFA may improve oxygenation.
 4.Corticosteroids stabilize cell member, PMN

adhesion, prevent surfactant reduction, protect

capillary endothelium, compliment activation and
minimize transudation.
CORTICOSTEROIDS

Value in ARDS of Fat embolism, aspiration,

sepsis, shock and cerebral edema.

Helpful in late stage in recovering patients in

reducing fibrotic change.

Improve and preserve arterial oxygenation and

stimulate proliferation and maturation of Type II
pneumocyte.
CORTICOSTEROIDS -

Prophylactic dose 10mg/Kg Q8H

Or

80mg/kg bolus

Or

1-2gm IV over 24 hrs. & maintain for 48-96 hrs by

gradual reduction
ATLS Protocol :

1. Early immobilization of fracture and early definitive

reduction (open or closed).

2. Maintain intravascular volume to maintain

cardiovascular stability (hypovolemic shock
resuscitation), may use colloids (albumin) as it can
expand fluid and bind FFA.

3. Mechanical ventilation with PEEP

 4. IV Ethanol has been used in Russia, Europe and
some American centres to decrease rate of FES.
J Bone Joint Surg Am. 1977 Oct;59(7):878-80

A raised level of alcohol in the blood was

associated with a lower incidence of fat embolism all
other variables controlled.

- Other studies
- Can J Surg. 1970 Jan;13(1):41-9

- Br Med J. 1978 May 13;1(6122):1232-4

ROLE OF FRACTURE STABILIZATION

Highly debated issue

- Accumulated evidence over past decade support

early fixation within 24 hours of injury.
 Early IF decompress # hematoma as ongoing
source of fat emboli and retained necrotic debris,
eliminate pain and physiologic stress with continued
# motion, optimize pulmn function, contributes to
reduced ventilatory dependence and improve
survival.
 But transient increasing pulmn Ar pressure and
worsening pulmn gas exchange observed during
reaming of medullary canal. So undreamed nailing
is suggested for femoral fixation in multiple #
patients.
PROGNOSIS
Mild -undetected
Mod -low mortality

Severe -fatal unless if treatement

instituted early. Survivors have pulmonary sequele.